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Open AccessJournal ArticleDOI

The role of tenascin-C in tissue injury and tumorigenesis.

TLDR
Hopes are generated that increased knowledge about tenascin-C will further improve management of diseases with high tenascInC expression such as chronic inflammation, heart failure, artheriosclerosis and cancer.
Abstract
The extracellular matrix molecule tenascin-C is highly expressed during embryonic development, tissue repair and in pathological situations such as chronic inflammation and cancer. Tenascin-C interacts with several other extracellular matrix molecules and cell-surface receptors, thus affecting tissue architecture, tissue resilience and cell responses. Tenascin-C modulates cell migration, proliferation and cellular signaling through induction of pro-inflammatory cytokines and oncogenic signaling molecules amongst other mechanisms. Given the causal role of inflammation in cancer progression, common mechanisms might be controlled by tenascin-C during both events. Drugs targeting the expression or function of tenascin-C or the tenascin-C protein itself are currently being developed and some drugs have already reached advanced clinical trials. This generates hope that increased knowledge about tenascin-C will further improve management of diseases with high tenascin-C expression such as chronic inflammation, heart failure, artheriosclerosis and cancer.

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Journal ArticleDOI

Matricellular Proteins in Cardiac Adaptation and Disease

TL;DR: Understanding the role of matricellular proteins in myocardial pathophysiology and identification of the functional domains responsible for their actions may lead to design of peptides with therapeutic potential for patients with heart disease.
Journal ArticleDOI

The Role of Cancer-Associated Fibroblasts and Fibrosis in Liver Cancer

TL;DR: The functional contributions of myofibroblasts, CAFs, and fibrosis to the development of HCC and CCA in the hepatic PME and TME are discussed, focusing on my ofibroblast- and extracellular matrix-associated growth factors, fibrosis-associated immunosuppressive pathways, as well as mechanosensitive signaling cascades that are activated by increased tissue stiffness.
Journal ArticleDOI

Tenascin-C at a glance.

TL;DR: Tenascin-C is an extracellular matrix molecule that shapes cell behavior in developing and traumatized tissues, and has a great potential in disease diagnosis and tissue repair.
Journal ArticleDOI

Advances in tenascin-C biology

TL;DR: The molecular mechanisms by which tenascin-C mediates these effects and the implications of mis-regulated tenascInC expression in driving disease pathology are highlighted.
Journal ArticleDOI

Tissue mechanics promote IDH1-dependent HIF1α-tenascin C feedback to regulate glioblastoma aggression.

TL;DR: It is found that glioma aggression and patient prognosis correlate with HIF1α levels and the stiffness of a tenascin C (TNC)-enriched ECM, and this work suggests that elevated ECM stiffness can independently foster glioblastomas aggression and contribute to gliOBlastoma recurrence via bypassing the protective activity of IDH1 mutational status.
References
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Journal ArticleDOI

Inflammation and cancer

TL;DR: It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration.
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Mechanisms of angiogenesis and arteriogenesis.

TL;DR: The cellular and molecular mechanisms underlying the formation of endothelium-lined channels and their maturation via recruitment of smooth muscle cells (arteriogenesis) during physiological and pathological conditions are summarized, alongside with possible therapeutic applications.
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TL;DR: Owing to the importance of these tumour-associated phenotypes in metastasis and cancer-related mortality, targeting the products of such cellular plasticity is an attractive but challenging approach that is likely to lead to improved clinical management of cancer patients.
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NF-kappaB: linking inflammation and immunity to cancer development and progression.

TL;DR: The hypothesis is put forward that activation of nuclear factor-κB by the classical, IKK-β (inhibitor-of-NF-β kinase-β)-dependent pathway is a crucial mediator of inflammation-induced tumour growth and progression, as well as an important modulator of tumour surveillance and rejection.
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Antiangiogenic Therapy Elicits Malignant Progression of Tumors to Increased Local Invasion and Distant Metastasis

TL;DR: It is reported that angiogenesis inhibitors targeting the VEGF pathway demonstrate antitumor effects in mouse models of pancreatic neuroendocrine carcinoma and glioblastoma but concomitantly elicit tumor adaptation and progression to stages of greater malignancy, with heightened invasiveness and in some cases increased lymphatic and distant metastasis.
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